Bilgimol Chumappumkal, JosephSekayan, TroFalah, NiccaBarnes, Richard F. W.Flood, VeronicaDe Pablo Moreno, Juan AndrésDrygalski, Annette von2025-01-232025-01-232024Joseph, BC, Sekayan, T., Falah, N., Barnes, RFW, Flood, V., De Pablo-Moreno, JA, y von Drygalski, A. (2024). La anemia ferropénica intensifica el sangrado traumático y la mortalidad en ratones, y se puede aliviar con ácido tranexámico. Investigación y práctica en trombosis y hemostasia , 8 (6). https://doi.org/10.1016/J.RPTH.2024.1025432475-037910.1016/j.rpth.2024.102543https://hdl.handle.net/20.500.14352/115835This study was funded by Annette von Drygalski Discretionary Funds (University of California San Diego).Background. Clinical evidence suggests that anemia exacerbates traumatic bleeding and worsens outcomes. Objectives. To study the influence of iron deficiency anemia on traumatic bleeding, coagulopathy, and mortality. Methods C57BL/6J mice received an iron-deficient diet (8 weeks; ±1 mg intraperitoneal iron dextran 2 weeks before trauma). Control mice received a normal diet. Iron deficiency anemia was confirmed by hematocrit, red cell indices, and liver iron. Mice received saline or tranexamic acid (TXA; 10 mg/kg) just before liver laceration. Blood loss, coagulopathy (activated partial thromboplastin time, factor [F]II, FV, FVIII, FX, and fibrinogen), D-dimer, thrombin-antithrombin complexes, and plasmin-alpha-2-antiplasmin complexes were analyzed at 15 and 60 minutes, and a cytokine panel was performed at 60 minutes and 6 hours after trauma. Survival was monitored for 7 days. Results. Compared with nonanemic mice, anemic mice had lower hematocrit and hepatic iron content. Anemic mice experienced higher blood loss compared with nonanemic mice, which was reduced by TXA. Both groups developed traumatic coagulopathy characterized by activated partial thromboplastin time prolongation, thrombin-antithrombin complex formation, and depletion of FV, FVIII, and fibrinogen. TXA corrected the coagulopathy. However, plasmin-alpha-2-antiplasmin complex formation and D-dimers, markers of fibrinolysis, were higher in anemic mice and were not corrected by TXA. Seven-day survival was low in anemic mice, and rescued by TXA, but high in nonanemic mice without additional improvement by TXA. Among cytokines, only interleukin-6 increased, which was prevented by TXA most notably in anemic mice. Conclusion. These observations provide first and critical proof-of-principle evidence that anemia accelerates traumatic bleeding and increases mortality, which could be rescued by anemia correction (parenteral iron) or periprocedural TXA.engAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/journal articlehttps://doi.org/10.1016/j.rpth.2024.102543https://www.sciencedirect.com/science/article/pii/S2475037924002383?via%3Dihubopen access616.15591.11591.41636.91.02AnemiaBleedingBlood lossCoagulopathySurgeryTranexamic acidTraumafibrinolysisHematologíaSistema cardiovascularFisiología animal (Biología)Animales de laboratorioPatología veterinaria3205.04 Hematología3207.04 Patología Cardiovascular2401.13 Fisiología Animal3109.04 Medicina Interna3109.07 Patología